There is conclusive research evidence for Vitamin B12 deficiencies with dementia. Maintaining good levels of B12 has been shown to reduce the chances of dementia. Will taking a B12 supplement improve memory and cognition?
The jury is still out. My view is that we know levels of B12 are deficient, it should be supplemented.
Vitamin B12 plays a crucial role in brain health and cognitive function. Studies find it is critical for individuals with Alzheimer’s disease or cognitive decline. Why? B12 deficiency causes cognitive impairment.
Why Do Vitamin B12 Deficiencies with Dementia Exist?
- B12 Deficiency and Cognitive Impairment:
- Vitamin B12 deficiency leads to cognitive problems, memory loss, and even neurological damage. Deficiency is common in older adults and it may contribute to symptoms that mimic or exacerbate cognitive decline, including conditions like Alzheimer’s disease.
- People with Alzheimer’s or other forms of dementia have lower B12 levels compared to healthy individuals. Addressing a B12 deficiency in such cases can improve cognitive function.
- Homocysteine Levels:
- One of the key roles of B12 is to help regulate homocysteine, an amino acid that, when elevated, is thought to increase the risk of cognitive decline and Alzheimer’s disease. High levels of homocysteine are linked to an increased risk of AD, and B12 helps convert homocysteine into other substances, reducing its harmful effects.
- Some studies have found that supplementing with B12, along with folate (which also help lower homocysteine levels), slows cognitive decline in those with mild cognitive impairment. An abstract of one such study follows:
Objectives: To evaluate the combined action of folic acid and vitamin B12 supplementation on cognitive performance and inflammation in patients with Alzheimer’s disease (AD).
Design: This was a randomized, single-blind, placebo-controlled trial.
Participants: Patients (n=120) diagnosed clinically as probable AD and in stable condition from Tianjin Key Laboratory of Cerebrovascular and Neurodegenerative Diseases.
Measurements: Individuals were randomly divided into the intervention group (n=60, folic acid 1.2 mg/d + vitamin B12 50 μg/d) and the placebo group (n=60). Cognitive performance, blood folate, vitamin B12, one carbon cycle metabolite, and inflammatory cytokine levels were measured at baseline and after 6 months. The data were analyzed using linear mixed models for repeated measures.
Results: A total of 101 participants (51 in the intervention group and 50 in the placebo group) completed the trial. Folic acid plus vitamin B12 supplementation had a beneficial effect on the MoCA total scores (P=0.029), naming scores (P=0.013), orientation scores (P=0.004), and ADAS-Cog domain score of attention (P=0.008), as compared to those of the control subjects. Moreover, supplementation significantly increased plasma SAM (P<0.001) and SAM/SAH (P<0.001), and significantly decreased the levels of serum Hcy (P<0.001), plasma SAH (P<0.001), and serum TNFα (P<0.001) compared to in the control subjects.
Conclusions: Folic acid and vitamin B12 supplementation showed a positive therapeutic effect in Alzheimers patients who were not on a folic acid-fortified diet. The findings of this study help to delineate nutrient intervention as far as public health management for the prevention of dementia is concerned.
Abstract
Alzheimer’s disease (AD) is the most common form of dementia in the elderly population, affecting over 55 million people worldwide. Histopathological hallmarks of this multifactorial disease are an increased plaque burden and tangles in the brains of affected individuals.
Several lines of evidence indicate that B12 hypovitaminosis is linked to AD. In this review, the biochemical pathways involved in AD that are affected by vitamin B12, focusing on APP processing, Aβ fibrillization, Aβ-induced oxidative damage as well as tau hyperphosphorylation and tau aggregation, are summarized.
Besides the mechanistic link, an overview of clinical studies utilizing vitamin B supplementation are given, and a potential link between diseases and medication resulting in a reduced vitamin B12 level and AD are discussed. Besides the disease-mediated B12 hypovitaminosis, the reduction in vitamin B12 levels caused by an increasing change in dietary preferences has been gaining in relevance.
In particular, vegetarian and vegan diets are associated with vitamin B12 deficiency, and therefore might have potential implications for AD. In conclusion, our review emphasizes the important role of vitamin B12 in AD, which is particularly important, as even in industrialized countries a large proportion of the population might not be sufficiently supplied with vitamin B12.
Robert Rodgers PhD
Founder 2010
Alzheimers Recovery